REQUIRED VIOLA REPERTOIRE FOR THE PRIMROSE COMPETITION AND THE TERTIS COMPETITION

William Primrose (1903-1982) and Lionel Tertis (1876-1975) made the viola a grand instrument for public performances of solo and chamber music throughout their long and active lives characterized by a common passion for the viola. I, too, have been deeply inspired by their passion for the viola. I chose, therefore, for my doctoral performance project to feature works for viola from the required repertoire of the William Primrose and Lionel Tertis competitions of 2001 and 2003, respectively. For purposes of the performances, I divided selections from the combined repertoire for the William Primrose and Lionel Tertis competitions into three recitals. The first recital included Sonata, Opus 120, No.2 in E-flat Major (1894) by Johannes Brahms; Sonata, Opus 147 (1975) by Dmitri Shostakovich; and Sonata (1919) by Rebecca Clarke. These pieces represent standard components of the general repertoire for both the Primrose and Tertis competitions. The second recital was comprised of two works dedicated by their composers to Primrose: Lachrymae, Opus 48 (1950) by Benjamin Britten; and Concerto (1945) by Bela Bartok. The third recital included three pieces dedicated by their composers to Tertis: Sonata (1922) by Arnold Bax; Sonata in C Minor (1905) by York Bowen; and Sonata (1952) by Arthur Bliss. The goal of my preparation for these recitals was to emphasize a variety of techniques and, also, the unique timbre of the viola. For example, the works I selected emphasized high-position technique, which was not much used before the nineteenth century, and featured the lowest string (the C-string), which provides a beautifully somber and austere sonority characteristic of the viola. For these reasons, the selected works provided not only attractive and interesting pieces to study and perform but were also of educational merit.

SELECTED REPERTOIRE OF THE GILLET COMPETITION FROM 1996 TO 2006

There are many bassoon competitions around the world- and one of the most famous is the Gillet competition, sponsored by the International Double Reed Society. In 1981, it was established as an annual event, the "Femand Gillet Bassoon Competition"- a title expanded in 2000 to the "Femand Gillet-Hugo Fox Bassoon Competition." My goal was to explore the history of the competition, the availability of the repertoire selected for each competition, and the difficulties performing each piece. Through this journey, I was able to discover the variety of material chosen and how it was used, the quality, value, and the importance of the repertoire in each competition. For example, Ferdinand David's Concertino op.12, the style of the piece provides romantic, operatic type lyricism, a flashy presto section and finale, makes it as a standard romantic piece in the bassoon repertoire; Otmar Nussio's Variations on an Air by Pergolesi, contains a slow theme and few diverse variations, which provides a contemporary style music with the traditional music form and descriptive quality. The result of learning this repertoire proves that different styles of music in the competition demonstrate the artistry of the bassoon repertoire and music history in relationship of the development of the instrument. My first dissertation recital featured: Concerto for Bassoon, K. 191 by Wolfgang Amadeus Mozart; Concertino by Marcel Bitsch; Metamorphoses by Leslie Bassett; and Sonatine by Alexandre Tansman. My second recital featured: Concerto in E minor, RV 484 by Antonio Vivaldi; On the Summer Map of Stars by Gordon Kerry; Concertino Opus12 by Ferdinand David; Elegie by Jacques Hetu; and Interferences by Roger Boutry. My third recital featured: Cello Suite No.2 in D minor, BWV1008 by Johann Sebastian Bach; Combinaciones: Sonatina para Fagot y Piano by Salvador Ranieri; Andante e Rondo Ungarese Opus 35 by Carl Maria von Weber; and Variations on an Air by Pergolesi for Bassoon and Piano by Otmar Nussio.

ROLE OF ICAM-1-MEDIATED ENDOCYTOSIS IN ENDOTHELIAL FUNCTION AND IMPLICATIONS FOR CARRIER-ASSISTED DRUG DELIVERY

Intercellular adhesion molecule 1 (ICAM-1) is a transmembrane protein found on the surface of vascular endothelial cells (ECs). Its expression is upregulated at inflammatory sites, allowing for targeted delivery of therapeutics using ICAM-1-binding drug carriers. Engagement of multiple copies of ICAM-1 by these drug carriers induces cell adhesion molecule (CAM)-mediated endocytosis, which results in trafficking of carriers to lysosomes and across ECs. Knowledge about the regulation behind CAM-mediated endocytosis can help improve drug delivery, but questions remain about these regulatory mechanisms. Furthermore, little is known about the natural function of this endocytic pathway. To address these gaps in knowledge, we focused on two natural binding partners of ICAM-1 that potentially elicit CAM-mediated endocytosis: leukocytes (which bind ICAM-1 via β₂ integrins) and fibrin polymers (a main component of blood clots which binds ICAM-1 via the γ3 sequence). First, inspired by properties of these natural binding partners, we varied the size and targeting moiety of model drug carriers to determine how these parameters affect CAM-mediated endocytosis. Increasing ICAM-1-targeted carrier size slowed carrier uptake kinetics, reduced carrier trafficking to lysosomes, and increased carrier transport across ECs. Changing targeting moieties from antibodies to peptides decreased particle binding and uptake, lowered trafficking to lysosomes, and increased transport across ECs. Second, using cell culture models of leukocyte/EC interactions, inhibiting regulatory elements of the CAM-mediated pathway disrupted leukocyte sampling, a process crucial to leukocyte crossing of endothelial layers (transmigration). This inhibition also decreased leukocyte transmigration across ECs, specifically through the transcellular route, which occurs through a single EC without disassembly of cell-cell junctions. Third, fibrin meshes, which mimic blood clot fragments/remnants, bound to ECs at ICAM-1-enriched sites and were internalized by the endothelium. Inhibiting the CAM-mediated pathway disrupted this uptake. Following endocytosis, fibrin meshes trafficked to lysosomes where they were degraded. In mouse models, CAM-mediated endocytosis of fibrin meshes appeared to remove fibrin remnants at the endothelial surface, preventing re-initiation of the coagulation cascade. Overall, these results support a link between CAM-mediated endocytosis and leukocyte transmigration as well as uptake of fibrin materials by ECs. Furthermore, these results will guide the future design of ICAM-1-targeted carrier-assisted therapies.